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      Serum Galectin-3 level, not Galectin-1, is associated with the clinical feature and outcome in patients with acute ischemic stroke

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          Abstract

          Aim

          To study the diagnostic and prognostic role of serum galectin-1 (Gal-1) and -3 (Gal-3) in acute ischemic stroke (AIS) patients.

          Methods

          We enrolled 233 patients with first-ever acute ischemic stroke and 252 healthy controls in this study. The AIS severity was evaluated by National Institutes of Health Stroke Scale (NIHSS) scores. The serum Gal-1 and -3 levels were determined. All patients were followed for 1 years and the functional outcome were evaluated by modified Rankin Scale (mRS) scores.

          Results

          We found that AIS patients had higher serum Gal-1 and -3 levels than controls. The serum Gal-3 level was closely associated with the AIS severity indicated by NHSS and infarction volume. Serum Gal-3 levels were significantly higher in patients with a poor outcome indicated by mRS scores than those in patients with a good outcome. In contrast, the serum Gal-1 is not associated with the severity and outcome of acute AIS patients. Our in vitro studies show that Gal-3 knockdown with siRNA dramatically increased the culture neuron cell viability and reduced apoptosis under oxygen glucose deprivation treatment. Meanwhile, the pro-inflammatory cytokine expression decreased with the inhibition of Gal-3.

          Conclusion

          Our finding provides a novel biological marker, serum Gal-3, for monitor of acute AIS patients.

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          Most cited references33

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          The influence of gender and age on disability following ischemic stroke: the Framingham study.

          Margaret Kelly-Hayes, Alexa S Beiser, Carlos Kase … (2007)
          The magnitude of disability among elderly stroke survivors is substantial. There have been few community-based estimates of the contribution gender and older age make to stroke-related disability and outcome. Using the original Framingham Study cohort, we documented gender-specific neurological deficits and disability differences in stroke survivors at six months post-stroke. Logistic regression analyses were performed to estimate odds ratios, comparing men and women, and adjusting for age, and age and stroke subtype. Age and gender-matched controls were then compared to distinguish stroke-related disability from disability associated with general aging. Results showed that almost half (43%) of all elderly stroke survivors in the cohort had moderate to severe neurological deficits. In the crude analyses, women were more dependent in ADLs (33.9% vs 15.6%), less likely to walk unassisted (40.3% vs 17.8%), and living in nursing homes (34.9 % vs 13.3%). After adjusting for age and stroke subtype, it was older age that accounted for the severity of disability. When compared to age and gender-matched controls, stroke cases were significantly more disabled in all domains studied. In this elderly cohort, more women experienced initial strokes and were more disabled at 6 months post-stroke than men. However, older age at stroke onset, not gender or stroke subtype, was associated with greater disability. Health care providers need to understand that strokes occur later in life for women and that because of age, women are at greater risk for disability and institutionalization.
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            Systemic infection, inflammation and acute ischemic stroke.

            B McColl, N Rothwell, Brian F. Allan (2009)
            Extensive evidence implicates inflammation in multiple phases of stroke etiology and pathology. In particular, there is growing awareness that inflammatory events outside the brain have an important impact on stroke susceptibility and outcome. Numerous conditions, including infection and chronic non-infectious diseases, that are established risk factors for stroke are associated with an elevated systemic inflammatory profile. Recent clinical and pre-clinical studies support the concept that the systemic inflammatory status prior to and at the time of stroke is a key determinant of acute outcome and long-term prognosis. Here, we provide an overview of the impact of systemic inflammation on stroke susceptibility and outcome. We discuss potential mechanisms underlying the impact on ischemic brain injury and highlight the implications for stroke prevention, therapy and modeling.
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              Galectin-3 is required for resident microglia activation and proliferation in response to ischemic injury.

              Mélanie Lalancette–Hébert, Vivek Swarup, Jean Martin Beaulieu … (2012)
              Growing evidence suggests that galectin-3 is involved in fine tuning of the inflammatory responses at the periphery, however, its role in injured brain is far less clear. Our previous work demonstrated upregulation and coexpression of galectin-3 and IGF-1 in a subset of activated/proliferating microglial cells after stroke. Here, we tested the hypothesis that galectin-3 plays a pivotal role in mediating injury-induced microglial activation and proliferation. By using a galectin-3 knock-out mouse (Gal-3KO), we demonstrated that targeted disruption of the galectin-3 gene significantly alters microglia activation and induces ∼4-fold decrease in microglia proliferation. Defective microglia activation/proliferation was further associated with significant increase in the size of ischemic lesion, ∼2-fold increase in the number of apoptotic neurons, and a marked deregulation of the IGF-1 levels. Next, our results revealed that contrary to WT cells, the Gal3-KO microglia failed to proliferate in response to IGF-1. Moreover, the IGF-1-mediated mitogenic microglia response was reduced by N-glycosylation inhibitor tunicamycine while coimmunoprecipitation experiments revealed galectin-3 binding to IGF-receptor 1 (R1), thus suggesting that interaction of galectin-3 with the N-linked glycans of receptors for growth factors is involved in IGF-R1 signaling. While the canonical IGF-1 signaling pathways were not affected, we observed an overexpression of IL-6 and SOCS3, suggesting an overactivation of JAK/STAT3, a shared signaling pathway for IGF-1/IL-6. Together, our findings suggest that galectin-3 is required for resident microglia activation and proliferation in response to ischemic injury.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncotarget
                Journal ID (iso-abbrev): Oncotarget
                Journal ID (publisher-id): Oncotarget
                Journal ID (publisher-id): ImpactJ
                Title: Oncotarget
                Publisher: Impact Journals LLC
                ISSN (Electronic): 1949-2553
                Publication date Collection: 12 December 2017
                Publication date (Electronic): 25 May 2017
                Volume: 8
                Issue: 65
                Pages: 109752-109761
                Affiliations
                1 Department of Geriatric Medicine, The First Affiliated Hospital of Jilin University, Changchun, China
                2 Department of Electrical Diagnosis, The General Hospital of Fourth Hospital of Jilin University, Changchun, China
                3 Department of Thoracic Surgery, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
                4 Department of Neurology, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, China
                5 Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun, China
                Author notes
                Correspondence to: Song-Yan Liu, neuro_h3@ 123456sohu.com
                [*]

                These authors have contributted equally to this study

                Article
                Publisher ID: 18211
                DOI: 10.18632/oncotarget.18211
                PMC ID: 5752558
                PubMed ID: 29312645
                SO-VID: 44675723-0a31-4c41-93c5-b7c9fa11565c
                Copyright © Copyright: © 2017 Dong et al.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 3 February 2017
                Date accepted : 1 May 2017
                Categories
                Subject: Clinical Research Paper

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: ischemic stroke,galectin-3,prognosis
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: ischemic stroke, galectin-3, prognosis

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